Evidence map›Paper›PMID 42113451›Full record

ArticleScience China. Life sciences2026

Tumor cell-intrinsic TET3 restrains type I interferon signaling and anti-tumor immunity.

Lu Liu, Wenxuan Zhao, Tianbao Shang, Bo Xu, Mengyuan Wang, Xinze Li, Jie Min, Wenqi Xu, Hongjie Shen, Li Tan and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Science China. Life sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Lu LiuLongevity and Aging Institute, Zhongshan Hospital, Shanghai Key Laboratory of Medical Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, China.
Wenxuan ZhaoLongevity and Aging Institute, Zhongshan Hospital, Shanghai Key Laboratory of Medical Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, China.
Tianbao ShangLongevity and Aging Institute, Zhongshan Hospital, Shanghai Key Laboratory of Medical Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, China.
Bo XuLongevity and Aging Institute, Zhongshan Hospital, Shanghai Key Laboratory of Medical Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, China.
Mengyuan WangLongevity and Aging Institute, Zhongshan Hospital, Shanghai Key Laboratory of Medical Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, China.
Xinze LiLongevity and Aging Institute, Zhongshan Hospital, Shanghai Key Laboratory of Medical Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, China.
Jie MinLongevity and Aging Institute, Zhongshan Hospital, Shanghai Key Laboratory of Medical Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, China.
Wenqi XuLongevity and Aging Institute, Zhongshan Hospital, Shanghai Key Laboratory of Medical Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, China.
Hongjie ShenLongevity and Aging Institute, Zhongshan Hospital, Shanghai Key Laboratory of Medical Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, China.
Li TanCenter for Medical Research and Innovation, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Longevity and Aging Institute, Zhongshan Hospital, Shanghai Key Laboratory of Medical Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, China. litan@fudan.edu.cn.
Yujiang Geno ShiLongevity and Aging Institute, Zhongshan Hospital, Shanghai Key Laboratory of Medical Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, China. shiyujiang@fudan.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The ten-eleven translocation (TET) family genes, which encode 5-methylcytosine (5mC) dioxygenases, play a "double-edged sword" role in tumor initiation and progression. However, the functional role and molecular mechanism of tumor cell-intrinsic TET3 in anti-tumor immunity remain incompletely understood. Here, we uncover that TET3 mRNA expression was aberrantly elevated in multiple cancer types and correlated with poor overall survival. Transcriptomic analysis reveals that TET3 depletion upregulated the expression of innate immune response genes, including numerous interferon-stimulated genes (ISGs), in cancer cells. The expression levels of dsRNA sensors (i.e., MDA5 and RIG-I) were increased in TET3 KO or KD cells, while the biogenesis of endogenous dsRNA was not affected. Mechanistically, TET3 regulates type I interferon signaling by inhibiting STAT1 activation. Importantly, depletion of TET3 in B16F10 melanoma cells significantly curbed the synergistic tumor growth, accompanied by increased tumor-infiltrating CD4

Indexed as

DioxygenasesInterferon Type INeoplasmsProto-Oncogene ProteinsAnimalsCell Line, TumorDendritic CellsGene Expression Regulation, NeoplasticHumansImmunity, InnateMiceMice, Inbred C57BLSignal TransductionSTAT1 Transcription FactorDioxygenasesInterferon Type IProto-Oncogene ProteinsSTAT1 Transcription FactorTET3 protein, humananti-tumor immunitySTAT1TET3type I interferon signaling

Identifiers

PMID42113451

What Socratic holds

Textmetadata
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.